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Regulation of hepatic metabolic pathways by the orphan nuclear receptor SHP 总被引:5,自引:0,他引:5 下载免费PDF全文
Boulias K Katrakili N Bamberg K Underhill P Greenfield A Talianidis I 《The EMBO journal》2005,24(14):2624-2633
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Glucocorticoid signaling is perturbed by the atypical orphan receptor and corepressor SHP 总被引:6,自引:0,他引:6
Borgius LJ Steffensen KR Gustafsson JA Treuter E 《The Journal of biological chemistry》2002,277(51):49761-49766
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Zhou XE Suino-Powell KM Xu Y Chan CW Tanabe O Kruse SW Reynolds R Engel JD Xu HE 《The Journal of biological chemistry》2011,286(4):2877-2885
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The orphan nuclear receptor SHP regulates PGC-1alpha expression and energy production in brown adipocytes 总被引:1,自引:0,他引:1
Brown adipocytes increase energy production in response to induction of PGC-1alpha, a dominant regulator of energy metabolism. We have found that the orphan nuclear receptor SHP (NR0B2) is a negative regulator of PGC-1alpha expression in brown adipocytes. Mice lacking SHP show increased basal expression of PGC-1alpha, increased energy expenditure, and resistance to diet-induced obesity. Increased PGC-1alpha expression in SHP null brown adipose tissue is not due to beta-adrenergic activation, since it is also observed in primary cultures of SHP(-/-) brown adipocytes that are not exposed to such stimuli. In addition, acute inhibition of SHP expression in cultured wild-type brown adipocytes increases basal PGC-1alpha expression, and SHP overexpression in SHP null brown adipocytes decreases it. The orphan nuclear receptor ERRgamma is expressed in BAT and its transactivation of the PGC-1alpha promoter is potently inhibited by SHP. We conclude that SHP functions as a negative regulator of energy production in BAT. 相似文献
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Oiwa A Kakizawa T Miyamoto T Yamashita K Jiang W Takeda T Suzuki S Hashizume K 《Biochemical and biophysical research communications》2007,353(4):895-901
Small heterodimer partner (SHP; NR0B2) is an orphan nuclear receptor and acts as a repressor for wide variety of nuclear hormone receptors. We demonstrated here that mouse SHP mRNA showed a circadian expression pattern in the liver. Transient transfection of the mSHP promoter demonstrated that CLOCK-BMAL1, core circadian clock components, bound to E-box (CACGTG), and stimulated the promoter activity by 4-fold. Liver receptor homologue-1 (LRH-1; NR5A2) stimulated the mSHP promoter, and CLOCK-BMAL1 synergistically enhanced the LRH-1-mediated transactivation. Interestingly, SHP did not affect the CLOCK-BMAL1-mediated promoter activity, but strongly repressed the synergistic activation of CLOCK-BMAL1 and LRH-1. Furthermore, in vitro pull-down assays revealed the existence of direct protein-protein interaction between LRH-1 and CLOCK. In summary, this study shows that CLOCK-BMAL1, LRH-1 and SHP coordinately regulate the mSHP gene to generate the circadian oscillation. The cyclic expression of mSHP may affect daily activity of other nuclear receptors and contribute to circadian liver functions. 相似文献
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The major cytologic features seen in fine needle aspirates from two cases of fibrolamellar hepatocellular carcinoma were: liver-like tumor cells, characterized by plump, polygonal forms with eosinophilic, granular cytoplasm; large oval nuclei with extremely prominent solitary nucleoli; and parallel bands of fibrous tissue and fibrocytes seen within the tumor fragments. Other helpful features included intracytoplasmic hyaline globules and well-delineated pale bodies. Clinically, the tumors occurred in young patients with noncirrhotic livers and ran a more favorable course than do other types of hepatocellular carcinoma. 相似文献
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Isoform-specific null mutations were used to define the functions of three orphan members of the nuclear receptor superfamily, E75A, E75B, and E75C, encoded by the E75 early ecdysteroid-inducible gene. E75B mutants are viable and fertile, while E75C mutants die as adults. In contrast, E75A mutants have a reduced ecdysteroid titer during larval development, resulting in developmental delays, developmental arrests, and molting defects. Remarkably, some E75A mutant second instar larvae display a heterochronic phenotype in which they induce genes specific to the third instar and pupariate without undergoing a molt. We propose that ecdysteroid-induced E75A expression defines a feed-forward pathway that amplifies or maintains the ecdysteroid titer during larval development, ensuring proper temporal progression through the life cycle. 相似文献
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